Research Perspective|Volume 2, Issue 9|pp 621—626

Novel roles for JNK1 in metabolism

Bengt F. Belgardt^1,², Jan Mauer^1,², Jens C. Brüning^1,²

¹Institute for Genetics, Department of Mouse Genetics and Metabolism, Center for Molecular Medicine, University of Cologne (CMMC), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), 2 Department for Internal Medicine University of Cologne 50674 Cologne, Germany
²Max Planck Institute for the Biology of Ageing, 50674 Cologne, Germany

Received: July 5, 2010Accepted: August 29, 2010Published: August 31, 2010

Copyright: © 2010 Belgardt et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Activation of stress-kinase signaling has recently been recognized as an important pathophysiological mechanism in the development of diet-induced obesity, type 2 diabetes mellitus and other aging-related pathologies. Here, c-Jun N-terminal Kinase (JNK) 1 knockout mice have been shown to exhibit protection from diet-induced obesity, glucose intolerance, and insulin resistance. Nonetheless, the tissue-specific role of JNK1-activation in the development of the metabolic syndrome has been poorly defined so far. Recently, it was demonstrated that JNK1 signaling plays a crucial role in the central nervous system (CNS) and in the pituitary to control systemic glucose and lipid metabolism partially through regulation of hormones involved in growth and energy expenditure.